Being Alive; November 1992
Mark Katz, MD and reported by Jim Stoecker

Unlike the current generation of antivirals, tat inhibitors do work in chronically infected cells. In order to make new virus, HIV requires the presence of the tat gene. Tat is like the "master switch" of HIV; without it, very little if any new HIV can be made by a chronically infected cell. Also, tat released from infected cells seems to play a role in causing latent HIV in other infected cells to activate.

This antiviral is potentially a giant leap forward in our fight against HIV. A person infected with HIV may have thousands of cells with HIV in the nucleus and AZT, ddI, ddC cannot touch them. The tat inhibitor will ensure that no new virus can be made.

Several companies are working on tat inhibitors. Test tube studies have shown no resistance developing even after a year, so there is hope of avoiding the rapid development of resistance seen, for example, with the "L" drugs. The tat inhibitors have also been shown to be effective against AZT-resistant strains of HIV.

Human studies are now under way at the University of California, San Diego. A group of 18 people in the 50-500 T-cell range are taking one of three doses of tat inhibitor. Six people are taking either AZT or ddI. This is only a 12 week study so results should be known by the end of the year. We can only hope for good news about efficacy and lack of resistance and side effects. We need the next generation of antivirals to become the current generation as quickly as possible.
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